title: The pathology of neoatherosclerosis in human coronary implants bare-metal and drug-eluting stents.
abstract: OBJECTIVE
  Human coronary bare-metal stents (BMS) and drug-eluting stents (DES) from autopsy cases with implant duration >30 days were examined for the presence of neointimal atherosclerotic disease.
  
  
  BACKGROUND
  Neointimal atherosclerotic change (neoatherosclerosis) after BMS implantation is rarely reported and usually occurs beyond 5 years. The incidence of neoatherosclerosis after DES implantation has not been reported.
  
  
  METHODS
  All available cases from the CVPath stent registry (n = 299 autopsies), which includes a total of 406 lesions-197 BMS, 209 DES (103 sirolimus-eluting stents [SES] and 106 paclitaxel-eluting stents [PES])-with implant duration >30 days were examined. Neoatherosclerosis was recognized as clusters of lipid-laden foamy macrophages within the neointima with or without necrotic core formation.
  
  
  RESULTS
  The incidence of neoatherosclerosis was significantly greater in DES lesions (31%) than BMS lesions (16%; p < 0.001). The median stent duration with neoatherosclerosis was shorter in DES than BMS (DES, 420 days [interquartile range [IQR]: 361 to 683 days]; BMS, 2,160 days [IQR: 1,800 to 2,880 days], p < 0.001). Unstable lesions characterized as thin-cap fibroatheromas or plaque rupture were more frequent in BMS (n = 7, 4%) than in DES (n = 3, 1%; p = 0.17), with relatively shorter implant durations for DES (1.5 ± 0.4 years) compared to BMS (6.1 ± 1.5 years). Independent determinants of neoatherosclerosis identified by multiple logistic regression included younger age (p < 0.001), longer implant durations (p < 0.001), SES usage (p < 0.001), PES usage (p = 0.001), and underlying unstable plaques (p = 0.004).
  
  
  CONCLUSIONS
  Neoatherosclerosis is a frequent finding in DES and occurs earlier than in BMS. Unstable features of neoatherosclerosis are identified for both BMS and DES with shorter implant durations for the latter. The development of neoatherosclerosis may be yet another rare contributing factor to late thrombotic events.
authors.affiliation: CVPath Institute, Inc., Gaithersburg, Maryland, USA.
authors.forename: Gaku
authors.initials: G
authors.lastname: Nakazawa
authors.forename: Fumiyuki
authors.initials: F
authors.lastname: Otsuka
authors.forename: Masataka
authors.initials: M
authors.lastname: Nakano
authors.forename: Marc
authors.initials: M
authors.lastname: Vorpahl
authors.forename: Saami K
authors.initials: SK
authors.lastname: Yazdani
authors.forename: Elena
authors.initials: E
authors.lastname: Ladich
authors.forename: Frank D
authors.initials: FD
authors.lastname: Kolodgie
authors.forename: Aloke V
authors.initials: AV
authors.lastname: Finn
authors.forename: Renu
authors.initials: R
authors.lastname: Virmani
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D003324:Coronary Artery Disease / Q000209:etiology* / Q000473:pathology*; D054855:Drug-Eluting Stents / Q000009:adverse effects; D005260:Female; D006801:Humans; D008297:Male; D008670:Metals / Q000009:adverse effects*; D008875:Middle Aged; D058426:Neointima / Q000473:pathology*; D015607:Stents / Q000009:adverse effects*
chemical_list: D008670:Metals